A study of where and how an enzyme cuts DNA may have inadvertently revealed a basic principle of gene regulation, say researchers in Boston Children's Hospital's Program in Cellular and Molecular Medicine (PCMM). The study, reported in the journalCell, suggests that the cell can lock or "sandbox" genes and enzymes that act on them within loops of DNA and protein, confining their activity to minimize the risk of genetic disaster.

In our cells, DNA and its associated proteins—a combination called chromatin—are folded and wrapped in complex ways to form chromosomes. Researchers have long noted within a chromosome, the chromatin is organized into a series of loops. These loops can range in size from a few thousand to nearly 2.5 million base pairs, large enough to contain one or more complete genes.

The study team—led by co-first authors Jiazhi Hu, PhD, and Yu Zhang, PhD, and senior author Frederick Alt, PhD—believes these loops may form the backbone of a fundamental organizing principle for genomic processes.

Recent research has yielded new information about immune responses associated with--and potentially responsible for--protection from HIV infection, providing leads for new strategies to develop an HIV vaccine. Results from the RV144 trial, reported in 2009, provided the first signal of HIV vaccine efficacy: a 31 percent reduction in HIV infection among vaccinees. Since then, an international research consortium has been searching for molecular clues to explain why the vaccine showed this modest protective effect.

A new review outlines findings that hint at the types of immune responses a preventive HIV vaccine may need to induce. The article was co-authored by leaders in HIV vaccinology, including Anthony S. Fauci, M.D., director of the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health, and lead author Lawrence Corey, M.D., of the Fred Hutchinson Cancer Research Center.

Scientists at The Scripps Research Institute (TSRI) have found a way to change leukemia cells into leukemia-killing immune cells. The surprise finding could lead to a powerful new therapy for leukemia and possibly other cancers.

"It's a totally new approach to cancer, and we're working to test it in human patients as soon as possible," said senior investigator Richard A. Lerner, Institute Professor and the Lita Annenberg Hazen Professor of Immunochemistry at TSRI.

The findings, published this week in the Proceedings of the National Academy of Sciences, result from the discovery of a rare human antibody.

New research by Dana-Farber Cancer Institute scientists raises the prospect of cancer therapy that works by converting a tumor's best friends in the immune system into its gravest enemies.

In a study published in the journal Science, an international collaboration of investigators from Dana-Farber, Harvard Medical School, Boston Children's Hospital, and the University of Strasbourg uncovered a mechanism that allows key immune system cells to keep a steady rein on their more belligerent brother cells, thereby protecting normal, healthy tissue from assault. The discovery has powerful implications for cancer immunotherapy researchers say: by blocking the mechanism with a drug, it may be possible to turn the attack-suppressing cells into tumor-attacking cells.

"Our findings results suggest a new strategy for immune system-based therapies for cancer," says the study's senior author, Harvey Cantor, MD, of Dana-Farber and Harvard. "By targeting a genetic pathway in cells that ordinarily restrain the immune response to cancer, we may be able to convert them into cancer...

The Nantz National Alzheimer Center at Houston Methodist Hospital is part of a landmark clinical trial that looks at removing a key protein from the brain to prevent memory loss at least a decade before symptoms are noticed in healthy older adults.

The national trial is focused on an investigational treatment to reduce the impact of the protein beta amyloid. The A4 study, also known as the Anti-Amyloid Treatment in Asymptomatic Alzheimer's study, is for individuals ages 65 to 85 who are deemed at risk for Alzheimer's disease related memory loss, but who have not yet shown signs of the disease.

Using positron emission tomography (PET scans), researchers and clinicians have found that beta amyloid begins forming plaques in the brains of people with Alzheimer's disease 10-20 years before the initial symptoms of the disease. Scientists believe the accumulation of beta amyloid may play a key role in the eventual development of Alzheimer's-related memory loss, by inducing...

Immunotherapy for the treatment of cancer is rapidly evolving from therapies that globally and non-specifically simulate the immune system to more targeted activation of individual components of the immune system.

The net result of this targeted approach is decreased toxicity and increased efficacy of immunotherapy. The understanding of the checkpoint signalling pathway involving the programmed death 1 (PD-1) receptor and its ligands (PD-L1/2) in tumour-induced immune suppression has been a critical advancement in immunotherapeutic drug development.

Cell signalling through the PD-1 receptor upon binding the PD-L1 ligand attenuates immune responses and is exploited by both tumours and viruses. The PD-L1 Inhibitor Screening Assay Kit from AMSBIO is designed for screening and profiling inhibitors of this signalling.

Dengue is a mosquito-borne tropical disease currently endemic in more than 10 countries. According to the World Health Organization, 390 million people are infected by dengue every year.

The disease can be caused by one of the four types of dengue virus transmitted by theAedes aegypty mosquito, the main vector for dengue. In humans, symptoms of dengue infection include fever, headache, muscle and joint pain and a characteristic skin rash. In some cases, dengue infection can take a dangerous turn and develop into a life-threatening hemorrhagic fever and dengue shock syndrome.

A tetravalent vaccine that could protect against all four types of dengue virus is not available--and neither is one that could protect against a single type, for that matter. What is more, no specific treatment against dengue exists. Thus, researchers have sought strategies to reduce mosquito habitat or replication. Unfortunately, none of the approaches developed so far has been successful in eradicating the disease or diminishing the odds of being bitten by the mosquito.

Speaking today at the plenary session of the 7th Annual European Antibody Congress in Geneva, Dr. Anat Cohen-Dayag, President and CEO of Compugen Ltd. (NASDAQ: CGEN), presented Compugen's Antibody Target Discovery Platform, one of the Company's predictive discovery platforms for novel therapeutic targets. As part of her presentation covering the unique discovery capabilities of this platform, Dr. Cohen-Dayag presented experimental data demonstrating the potential of two in silicopredicted proteins, CGEN-928 and CGEN-15001T, to serve as new targets for monoclonal antibody ("mAb") based therapy.

A unique molecule developed at Duke Medicine, the University of North Carolina at Chapel Hill and MacroGenics, Inc., is able to bind HIV-infected cells to the immune system's killer T cells. It could become a key part of a shock-and-kill strategy being developed in the hope of one day clearing HIV infection.

The molecule is a type of bi-specific antibody known as a Dual-Affinity Re-Targeting protein, or DART®. It was engineered by MacroGenics, using HIV-targeting antibodies discovered at Duke. Employed increasingly in cancer research, bi-specific molecules have shown effectiveness in helping the immune system recognize and clear tumor cells. In this case, pre-clinical models demonstrate that DART creates a fatal union between HIV-infected cells and killer T cells.

When Julia Sung, M.D., lead author and clinical assistant professor in medicine at UNC, used DART molecules in combination with additional agents that wake up latent reservoirs of the virus hiding in the body, the approach showed early promise as a way to clear HIV infection.

The responses are especially noteworthy given the difficulty in treating MCC, which often evades the patient’s immune response. MCC is a rare but aggressive skin cancer linked to UV light exposure and the very common Merkel cell polyomavirus.

Durable responses to chemotherapy in the metastatic setting are not often achieved, with progression-free survival rates of around 90 days commonly observed.

However, MCC tumours express PD-L1, leading investigators to reason that this may provide an immunotherapeutic target, which could make MCC responsive to PD1 blockade.

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